We have shown that chronic hypoxic pulmonary hypertension is caused by structural remodeling. We are investigating the role of hypoxia per se and of other humoral and hemodynamic features in producing the structural changes. In the coming year we will explore the effect of superimposed change in pulmonary artery blood flow patterns. Hemodynamic monitoring and morphometric techniques will be applied. When analyzed by light microscopy, the timing and severity of the structural changes produced by hypoxia are found to be different in the infant from the adult lung. The ultrastructural features will be studied in the hilar artery of the hypoxic infant lung and compared with our earlier findings in the adult. Similarly the nature and amount of myosin in hilar and peripheral arteries will be compared in infant and adult, in normal and hypoxic animals.